The Emerging Role of ARID1A Expression and Its Promoter in Pathogenesis of Adenomyosis: a Narrative Review

Abstract

Adenomyosis is a benign gynecological condition characterized by the presence of endometrial glands and stroma within the myometrium. It affects reproductive-aged women and causes significant morbidity. Recent evidence suggests that downregulation and mutation of ARID1A, a tumor suppressor gene and its epigenetic alteration that cause chromatin remodeling complexes, play crucial roles in adenomyosis pathogenesis. This narrative review aims to synthesize current evidence on the Role of ARID1A Expression and Its Promoter in adenomyosis pathogenesis. A comprehensive literature search was conducted in PubMed, Web of Science, and Scopus databases for studies published between 2015 and 2025. Search terms included "adenomyosis," "ARID1A," "oxidative stress," "DNA methylation," "chromatin remodeling," and "epigenetics." Studies investigating the molecular mechanisms underlying adenomyosis, particularly those examining ARID1A function, oxidative stress, and DNA methylation patterns, were included. We found that there are complex relationships among oxidative stress, ARID1A expression, and DNA methylation in the pathogenesis of adenomyosis. The interactions between oxidative damage, chromatin dysfunction, and genomic instability suggest that adenomyosis is an epigenetic disease driven by oxidative stress.